Concerning the molecular mechanism of AF, besides the well‐known inhibition of thioredoxin reductase [8], other potential targets, including Inhibitory kB kinase, deubiquitinases, protein kinase C iota, and phosphatidylinositol 3‐kinase/protein kinase B (PI3K/Akt), have been proposed to explain the cytotoxic activity of this drug [1, 2]. The gene discussed is PRDX5; the disease is atrial fibrillation.